Background and purpose: Icariin (ICA) is the important active flavonoids extracted from Berberidaceae epimedium. It has been shown to be effective in suppressing cancers including lung cancer and gastric cancer. Thus

it is expected to be developed for cancer treatment. However

there were few studies on icariin as a promising anticancer drug for the treatment of thyroid cancer. The mechanisms underlying anticancer effects of ICA in thyroid cancer are rarely reported. This study was to explore the proliferation and apoptosis

intracellular ROS and antioxidant enzyme systems of the thyroid carcinoma cell line B-CPAP treated with different concentrations of ICA. It aimed to explore the mechanism underlying anticancer effects of ICA

and to determine whether it is concentrationor time-dependent manner. Methods: The proliferation of B-CPAP cell line treated with different concentrations of ICA was detected by cell counting kit-8 (CCK-8). The cell apoptosis and intracellular ROS were observed by flow cytometry. The expression of intracellular superoxide dismutase and intracellular malondialdehyde were measured by SOD detection kit and MDA assay kit

respectively. Bcl-2 and γ-HA2X were detected by Western blot. Results: ICA reduced B-CPAP cell activity

increased the rate of apoptosis in a dose- and time-dependent manner after 48 h (P0.01). The ROS of ICA 50 mg/L and 200 mg/L groups were (2.12±0.14)-fold and (2.41±0.12)-fold of the control group

respectively. ICA promoted accumulation of malondialdehyde

and reduced antioxidant enzyme SOD activity. The SOD activity was decreased by (9.35±1.45)% (ICA 50 mg/L group) and (21.5±1.52)% (ICA 200 mg/L group) compared with the control group

respectively. The anti-apoptotic protein Bcl-2 in ICA 200 mg/L group was decreased by (13.64±1.71)% compared with the control group. Conclusion: Icariin inhibited activity of thyroid cancer B-CPAP cells in a dose- and time-dependent manner. It plays an important role in promoting intracellular ROS expression

inhibiting superoxide dismutase expression and decreasing Bcl-2

which leads to irreversible damage to the cell

thereby inducing apoptosis.